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Weak sinusoidal electric fields modify the calcium efflux from freshly isolated chick and cat cerebral tissues bathed in Ringer's solution, at 360. Following incubation (30 min) with radioactive calcium (45Ca2+), each sample, immersed in fresh solution, was exposed for 20 min to fields at 1, 6, 16, 32, or We have previously described a sharply increased efflux of calcium from isolated chick brain tissues exposed to modulated radio frequency fields (16). These studies showed that the response depended on a narrow band of slow modulation frequencies (6-25 Hz), and not on the presence of the unmodulated carrier wave alone (147 MHz, 0.8 mW/cm2). In the present study, chick cerebral hemisphere and cat cerebral cortex were exposed, in vitro, to weak (5-100 V/m) extremely low frequency (ELF) fields (1-75 Hz). MATERIALS AND METHODSField exposure was performed in an environmental screened chamber, between two parallel metal plates, one square meter in area, 50 cm apart. Sine wave electric fields were applied to the plates at levels of 5-100 V/m and at frequencies of 1-75 Hz. Equal voltages with respect to ground were applied to each plate.Chick cerebral hemispheres were rapidly removed following decapitation. The hemispheres were separated and after weighing each was incubated at 36' for 30 min in 1 ml of a physiological medium [155 mM NaCl, 5.6 mM KCI, 2.16 mM CaCl2, 24 mM NaHCO3, and D-glucose (2 g/liter)] together with 0.2 ml of a solution containing 45Ca2+ (0.2 1ACi, specific activity 1.39 Ci/mmol). The incubated samples were then rinsed three times and exposed for 20 min to an environmental electric field while immersed in 1.0 ml of the physiological medium. At the conclusion of field exposure, an aliquot of 0.2 ml of the bathing solution was taken for scintillation counting. Prior to counting this aliquot was mixed with 9.0 ml of a scintillation adjuvant (Packard Dimilume). The brain samples were dissolved overnight in a digestive medium (Soluene 350, Packard) and then assayed for radioactivity. For each field condition (in both frequency and amplitude) "sets" of 10 brain samples were used simultaneously in field exposure and control conditions. Control samples were tested identically to the test samples except for the field exposure. All tissues were maintained at 36' during the whole experiment (16).The same experimental procedure was applied to striated muscles (lateral head of the gastrocnemius) in a series of chicks to evaluate possible effects in nonnervous tissue. Fifty muscle specimens were tested with 20 V/mi, 16 Hz field and compared with nonexposed muscles (30 samples). The statistical treatment of the data was identical to that applied to brain tissues.Samples of freshly removed cat cortex were similarly tested. Under ether anesthesia, the cerebral hemispheres were exposed. After completion of surgery, general anesthesia was discontinued and local anesthesia was instituted in all incisions and pressure points and thereafter the animal was immobilized with gallamine triethiodide (6.0 mg, intra...

Low-energy electromagnetic fields pulsed at frequencies of 10-90 Hz significantly increase healing ofchronic fracture nonunions in man. These fields are effective at tissue current levels several orders of magnitude lower than those required for transmembrane depolarization ofnormal cells. We have examined the effects of two clinically used pulsed electromagnetic fields on cultures of the osteoblast-like mouse bone cell line MMB-1. Both fields significantly reduced cellular production of cAMP in response to parathyroid hormone and osteoclast activating factor. Neither basal nor fluoride-activated levels of adenylate cyclase were altered in membranes from cells cultured in the fields; however, the same membrane -preparations exhibited markedly inhibited responses to parathyroid hormone. The fields blocked the inhibitory effects of the hormone on collagen synthesis by MMB-1 cells. However, there was no effect on the inhibition of collagen synthesis by 1,25-dihydroxyvitamin D3, which is believed to act primarily by a nuclear, rather than by a membrane-dependent, mechanism. No significant differences were noted between effects of the two fields, one generating continuous pulse trains (72 Hz) and the other generating recurrent bursts (15 Hz) of shorter pulses. We hypothesize that these field effects are mediated primarily at the plasma membrane of osteoblasts, either by interference with hormone-receptor interactions or by blocking of receptor-cyclase coupling in the membrane. These responses occurred with induced extracellular fields of 1 mV/cm or less, even though transmembrane potential gradients are typically 105 V/cm.Clinical studies (1-5) have demonstrated the usefulness ofelectromagnetic fields in stimulatinghealing ofchronically ununited fractures in humans. Devices generating such fields have been approved for clinical use. However, the mechanisms of action of these fields are not clear. Oscillating electromagnetic fields proven effective in clinical use generate electrochemical gradients in the tissue fluid surrounding cells (6), but these gradients are considerably weaker than the levels required to depolarize cell membranes. Typically, the devices in question impose -20-G pulsed magnetic fields, which induce current densities of -1 uA/cm2 and associated electric gradients of 1-10 mV/cm in extracellular fluids (2). Because of the high resistance ofcell membranes, any transmembrane electrical components ofimposed fields would be lower than the extracellular gradients by two to three orders of magnitude (6) and thus as much as six orders of magnitude less than the typical excitatory threshold currents of 1 mA/cm2 observed for axonal depolarization (7).It would therefore appear that the effectiveness ofsuch weak stimuli in generating cellular processes must depend on a series of amplification mechanisms, either before or during the transmembrane coupling of the initial stimulus (8). Likely loci for amplification and extension of weak electrochemical triggering events at the cell membrane may involve ...

We have tested an 836.55 MHz field with North American Digital Cellular (NADC) modulation in a 2-year animal bioassay that included fetal exposure. In offspring of pregnant Fischer 344 rats, we tested both spontaneous tumorigenicity and the incidence of induced central nervous system (CNS) tumors after a single dose of the carcinogen ethylnitrosourea (ENU) in utero, followed by intermittent digital-phone field exposure for 24 months. Far-field exposures began on gestational day 19 and continued until weaning at age 21 days. Near-field exposures began at 35 days and continued for the next 22 months, 4 consecutive days weekly, 2 h/day. SAR levels simulated localized peak brain exposures of a cell phone user. Of the 236 original rats, 182 (77%) survived to the termination of the whole experiment and were sacrificed at age 709-712 days. The 54 rats (23%) that died during the study ("preterm rats") formed a separate group for some statistical analyses. There was no evidence of tumorigenic effects in the CNS from exposure to the TDMA field. However, some evidence of tumor-inhibiting effects of TDMA exposure was apparent. Overall, the TDMA field-exposed animals exhibited trends toward a reduced incidence of spontaneous CNS tumors (P < 0. 16, two-tailed) and ENU-induced CNS tumors (P < 0.16, two-tailed). In preterm rats, where primary neural tumors were determined to be the cause of death, fields decreased the incidence of ENU-induced tumors (P < 0.03, two-tailed). We discuss a possible approach to evaluating with greater certainty the possible inhibitory effects of TDMA-field exposure on tumorigenesis in the CNS.